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As one of the most common cancers in female, ovarian cancer (OC) has become a serious public burden now. Mounting researches have indicated long noncoding RNAs (lncRNAs) can affect many biological processes including cancer development. LncRNA LBX2-AS1 was identified to be an oncogene in some cancers, but the role of LBX2-AS1 in OC remains to be elucidated. Bioinformatics analysis and experiments including ChIP, RT-qPCR, RIP, luciferase reporter, western blot and CCK-8 were performed to explore the role of LBX2-AS1 in OC. LBX2-AS1 expression was markedly increased in OC tissues and cell lines. Functionally, LBX2-AS1 silencing inhibited cell proliferation, migration and stemness but facilitated cell apoptosis in OC. Moreover, depletion of LBX2-AS1 suppressed tumor growth of OC in vivo. Mechanically, LBX2-AS1 was activated by transcriptional factor ELK1. ELK1 enhanced the expression of LBX2-AS1 in OC cells. In addition, miR-4784 was confirmed to be sponged by LBX2-AS1. There was a negative expression correlation between LBX2-AS1 and miR-4784 in OC tissues. Subsequently, KDM5C was identified to be a direct target of miR-4784 in OC cells. KDM5C was negatively regulated by miR-4784 and positively regulated by LBX2-AS1 in terms of expression level. Upregulation of KDM5C reversed the inhibitory effect of LBX2-AS1 depletion on the progression of OC. This study proved that ELK1 activated-LBX2-AS1 aggravated the progression of OC by targeting the miR-4784/KDM5C axis, suggesting that LBX2-AS2 may be a promising diagnostic biomarker of OC.

Purpose: To investigate the expression of rhotekin 2 (RTKN2) in human endometrial carcinoma tissues and its role in cancer progression. Methods: Quantitative polymerase chain reaction (qPCR) and immunoblot assays were performed to determine the expression of RTKN2 in endometrial carcinoma tissues and cells. The effects of RTKN2 on cell proliferation were assessed using cell counting kit-8 and EdU assays, while its effects on cell cycle and apoptosis in endometrial carcinoma cells were evaluated by flow cytometry. The involvement of RTKN2 in activating Akt/glycogen synthase kinase-3 beta (GSK3β) pathway was characterized using an immunoblot assay. Tumor growth assays were performed to assess the effects of RTKN2 on the progression of endometrial carcinoma in vivo, while protein expression in tumor tissues was determined by an immunohistochemical assay. Results: High expression of RTKN2 was found in human endometrial carcinoma tissues and cell lines (p < 0.05). RTKN2 promoted the proliferation and cell cycle of endometrial carcinoma cells in vitro and suppressed apoptosis (p < 0.05). RTKN2 also activated Akt/GSK3β pathway in endometrial carcinoma cells and thus promoted tumor growth in vivo. Conclusion: The involvement of RTKN2 in the progression of endometrial carcinoma has been confirmed in this study. RTKN2 is thus a promising therapeutic target for patients with this disease.

Ovarian cancer is the most lethal disease among the malignant tumors of female reproductive organs. Few successful therapeutic options exist for patients with ovarian cancer. The common therapeutic methods are surgical operation, chemotherapy, radiotherapy, and combination of these treatments. In recent years, studies have indicated that Pinellia pedatisecta Schott (PPS), a traditional Chinese medicine, could inhibit tumor growth. In this study, we demonstrated that PPS extract could induce apoptosis in SKOV3 cells in a dose- and time-dependent manner. We further conducted transcriptome sequencing on PPS extract-treated SKOV3 cells along with controls, and identified 1,754 transcripts whose expression differs at least 3-fold over the controls. These differentially expressed transcripts include the apoptosis-related genes such as the caspase family members, and were significantly enriched in steroid biosynthesis in the KEGG pathway database compared with the transcriptome background. Most of the differentially expressed transcripts from this pathway were upregulated in PPS extract-treated cell line, indicating that PPS extract-induced apoptosis was accompanied by increased steroid biosynthesis (e.g. zymosterol). These results suggest that PPS extract could be a new cytostatic therapeutic agent for ovarian cancer.